Thursday, September 16, 2010

SICU Rounds Report - Sept 8th, 2010

Candida in Urine. Remember that candida is a normal part of the GU/GI flora. Finding some in the urine is therefore a very common finding in the ICU (prevelance 40% in one series). The huge majority (95%) are asymptomatic. Whether it represents colonization or infection is uncertain. Fungal counts don't appear to correlate. Many patients that are chronically catheterized have white cells in their urine anyway. When found, most (>50%) is C. albicans. Almost all patients have foleys and are on antibiotics. About half have diabetes or preexisting urinary tract issues.
Infectious Diseases Society of America (IDSA) published guidelines for the treatment of candidiuria in 2009 which say:
  • Uncomplicated, asymptomatic funguria shouldn't be treated because it will likely recur and is unlikely to lead to dissemination or kidney infection
  • Symptomatic fungus (pain, dysuria) should be treated
  • Those with urinary tract abnormalities or procedures (pre or post) should be treated and proably imaged.
  • If spread to kidneys (flank pain, CVA tenderness, abd pain) treat

Richards, MJ, Edwards, JR, Culver, DH, Gaynes, RP. Nosocomial infections in medical intensive care units in the United States. National Nosocomial Infections Surveillance System. Crit Care Med 1999; 27:887.
Pappas, PG, Kauffman, CA, Andes, D, et al. Clinical practice guidelines for the management of candidiasis: 2009 update by the Infectious Diseases Society of America. Clin Infect Dis 2009; 48:503.

Methamphetamine Chronic Effects. Worldwide, methamphetamine is the most commonly abused drug (unless you count alcohol, tobacco, caffeine or cannabis). Acutely, it is a potent stimulant similar to ephedrine and causes all manner of neuro/CV/Pulm excitement: agitation, psychosis, tachypnea, tachycardia, hypertension. With severe intoxication worry about coma, shock, body temperature >39ÂșC, acute renal failure, metabolic acidosis, and hyperkalemia. (Note to Patrick - succhinylcholine is contraindicated in these patients!). Recommended treatment of acute intoxication is benzos, maybe haldol if needed. It seems like for the tachycardic hypertensive patient, precedex might hit the spot, but I would avoid a bolus as it rarely can cause hypertension.  Chronically, the effects are primarily in the head - memory loss, loss of executive function, etc. Cardio- and Neuro-Vascular problems (ICH, CHF, aneurysm of the aorta) have been described with chronic use. Withdrawal occurs hours after stopping and peaks at 1-2 days. Symptons of withdrawal are all in the CNS: drug craving, depression, insomnia, agitations, fatigues, etc.
2009 World Drug Report, Volume 1: Analysis. United Nations Office on Drugs and Crime. Available online at: (Accessed on Sept 8th, 2010)
Meredith, CW, Jaffe, C, Ang-Lee, K, Saxon, AJ. Implications of chronic methamphetamine use: a literature review. Harv Rev Psychiatry 2005; 13:141.

From Scott:
Pheochromocytoma Testing. A pheo should be be suspected in patients who have one or more of the following self-limited episodes of nonexertional palpitations, diaphoresis, headache, tremor, or pallor, resistant hypertension (especially at a young age), MEN2, fam hx, adrenal masses.  The only interfering medication is Levodopa, which can cause falsely elevated DA levels (B-Blockers should still be fine). Recommended tests are plasma metanepherines in PTs with family history, etc, who are at high risk (high pre-test probability) of having a Pheo or 24hr urine metanephrines in pts with a low pre-test probability.

From Chris:
Ranexa (ranolazine) is a piperazine derivative used for the treatment of chronic angina.  The dose begins at 500mg BID and then increases to 1000mg BID if symptoms continue.  It can not be used with any drug that induces or inhibits CYP3A or in people with hepatic dysfunction.  It can cause QTc prolongation, as well has occasional (0.5-2% incidence) bradyarrhthmia, hypotension and syncope.  It has the standard common GI side effects (upset, constipation, nausea etc).  It also has a HUGE list of drug interactions  Because of these things it is not a 1st choice drug.  Studies show that it can decrease angina frequency and nitro use when combined with beta-blockers, nitrates, Ca channel blockers and/or other HTN medications.  It can also increase exercise duration when combined with amlodipine.

The mechanism isn't clearly known.  But, the anti-anginal effect may be due to the prolongation of the ventricular action potential.  It inhibits the inactivating component of the Na flow and the rapidly rectifying K flow.  There is also thinking that it might incrase cardiac ATP supply by inhibiting fatty acid oxygenation (thereby forcing the myocardium to use more glucose).  But, it's not known if or how this directly relates to it's anginal effects.

Finally, there was thought that it may be useful in acute MI.  But, studies show that it provides no benefit, and is insanely expensive.  So there's no indication for this use.
Micromedex DRUGDEX database
Abdallah H. & Jerling M.: Effect of hepatic impairment on the multiple-dose pharmacokinetics of ranolazine sustained-release tablets. J Clin Pharmacol 2005; 45(7):802-809.
Thadani U, Ezekowitz M, Fenney L, et al: Double-blind efficacy and safety study of a novel anti-ischemic agent, ranolazine, versus placebo in patients with chronic stable angina pectoris. Circulation 1994; 90:726-734.

From Patrick:
Stim Test. ACTH (or cosyntropin) is normally produced by the pituitary and stimulates adrenal
glands to release cortisol. The stim test is a measure of how well the adrenal glands respond to ACTH to produce cortisol. There are two versions of the test, the short and long test.
The conventional short test compares serum cortisol levels before and after administration of 250ug ACTH; if the cortisol level one hour after administration of ACTH is >170 nmol/L and has risen by at least 330 nmol/L – 690 nmol/L, adrenal failure is excluded. If not, then there is some degree of adrenal failure and the long test is then used to distinguish between primary and secondary adrenal failure.

The long test involves administering higher doses of ACTH (1mg of synthetic ACTH) and cortisol levels are then checked at 1, 4, 8, and 24 hours later. Normally, cortisol levels should reach 1000 nmol/L by 4 hours. In primary adrenal insufficiency, cortisol levels are reduced at all stages whereas in secondary adrenal insufficiency, cortisol levels reach normal levels but take longer to reach those levels.

Some studies showed that a lower dose of ACTH (1ug) can be used when performing the
short stim test, and that the 30-min cortisol response is constant and unrelated to basal cortisol level or time of day; therefore, administering 1ug of ACTH and then measuring cortisol 30-min after is a safe and more sensitive way to perform the short ACTH stim test as compared to the conventional 250ug dose of ACTH.

Another study using synacthen (synthetic ACTH) directly compared the low dose short synacthen test (1ug of ACTH) with the conventional dose short synacthen test (250ug of ACTH) to the standard test of the hypothalamic-pituitary-adrenal axis, the insulin tolerance test (ITT).  They found that, at a cortisol cut-off level of 600 nmol/L (greater than that indicates adequate adrenal response) the low dose short synacthen test (LDSST) had 100% sensitivity (better than the 250ug short synacthen test [SST]) without any false negatives, and that there was a high correlation between peak cortisol response in the LDSST and the 30min cortisol level in the SST.  The authors recommend that, because of the greater sensitivity and less false negatives, the LDSST may replace both the ITT and the SST for initial evaluation of the HPA axis in patients with pituitary disease.  They suggest using 1ug tetracosactrin (synthetic ACTH) with cortisol sampling at 0, 20, and 30min after administration (3).
Dickstein G, Shechner C, Nicholson WE, Rosner I, Shen-Orr Z, Adawi F, Lahav M. Adrenocorticotropin stimulation test: effects of basal cortisol level, time of day, and suggested new sensitive low dose test. J Clin Endocrinol Metab. 1991 Apr;72(4):773-8.
Dickstein, Gabriel M.D.; Arad, Eldad M.D.; Shechner, Carmela M.D. Low-Dose ACTH Stimulation Test. The Endocrinologist. 1997 7(5).
Abdu TA; Elhadd TA; Neary R; Clayton RN. Comparison of the low dose short synacthen test (1 microg), the conventional dose short synacthen test (250 microg), and the insulin tolerance test for assessment of the hypothalamo-pituitary-adrenal axis in
patients with pituitary disease. J Clin Endocrinol Metab. 1999; 84(3):838-43

Also from Patrick:
Speaking Valves. These are one way valves that are placed on deflated, cuffless tracheostomy tubes and remain open during inhalation and close during exhalation (via a thin, flexible silicone diaphragm that moves to the open position during inhalation and is pushed closed during exhalation).  This not only allows for natural voicing and uninterrupted phonation but also reduces secretions and makes them easier to manage (less suctioning needed) by allowing the user to cough and expectorate orally.  Also expedites the decannulation process and restores sense of smell and taste (good for increasing appetite).

Contraindications to using a speaking valve include: severe upper airway obstruction, tenacious pulmonary secretions, decreased cognitive status, and are incompatible with foam filled, cuffed tracheostomy tubes.
Info from U-Miami library site: based on info from Mason MF. Speech Pathology for Tracheostomized and Ventilator Dependent Patients. Newport Beach, CA, Voicing, 1993 and Hoit JD and Shea SA. Speech production and speech with a phrenic nerve pacer. American Journal of Speech-Language Pathology 1996 5(2):53-60 May

From Max:
TPN vs PPN: Patients should be fed because underfeeding in ICU patients is associated with increased morbidity and mortality.   Use of the GI tract is encouraged because septic complications may be reduced and gut villi better preserved with administration of at least some nutrients into the GI tract.  All patients who are not expected to be on normal nutrition within 3 days should receive parenteral nutrition (PN) within 24-48 h if enteral nutrition (EN) is contraindicated (bowel obstruction, short bowel syndrome, abdominal compartment syndrome, mesenteric ischemia) or if they cannot tolerate EN.

PN should only be initiated in patients who are hemodynamically stable and who are able to tolerate the fluid volume, protein, carbohydrate, and lipid doses necessary to provide adequate nutrients.  Access for parenteral nutrition is generally obtained by placement of a central venous catheter (TPN). TPN provides carbohydrates in the form of glucose, protein in the form of amino acids, lipids in the form of triglycerides, electrolytes, vitamins and trace minerals. Major complications are bloodstream infections and adverse metabolic effects (hyperglycemia, refeeding syndrome). Most PN solutions are hypertonic to body fluids. If not administered into a high flow venous system (vena cava), it may cause venous thrombosis, thrombophlebitis, and extravasation.

Catheter tip placement elsewhere than the vena cava is considered peripheral access. In PPN, veins of hand or forearm are usually used. Veins of the lower limb are occasionally used if those of the upper limbs are not accessible. The osmolarity of the fluids delivered are lower than that of conventional parenteral nutrition (<850 mOsm/L). It's typically used for short periods (up to two weeks). Lipid emulsion appears to provide protection to the vein and allows tolerance to higher osmolarity infusions. PPN is useful for hypocaloric support with low to moderate protein provision, transitional support until central access can be obtained, and temporary support until catheter replacement following recurrent catheter-related sepsis. Major complication is thrombophlebitis.
Singer et al. ESPEN Guidelines on Parenteral Nutrition: Intensive care. Clinical Nutrition 2009; 28: 387–400
Rollins, C. Peripheral Parenteral Nutrition.

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